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Summary Objectives The aims of this study were to determine the mechanism of an outbreak of measles in adults and to provide scientific measures for putting forward a measles elimination program. Methods We performed a cross-sectional investigation during the measles outbreak to identify a possible communication link. Results From November 1, 2011 to January 26, 2012, the town reported 11 cases of measles in total. The case study identified an obvious propagation chain, which showed ordered and intimate exposure between cases. Conclusions Hospital exposure 1–2 weeks before infection with measles was the main cause of the measles outbreak. We must be fully aware of the possibility of nosocomial infection in an outbreak of measles; controlling nosocomial infections is a vital step in the prevention and control of the propagation of measles. [ABSTRACT FROM AUTHOR]

Neurogenesis in the adult brain is well recognized and plays a critical role in the maintenance of brain function and homeostasis. However, whether neurogenesis also occurs in the adult peripheral nervous system remains unknown. Here, using sensory ganglia (dorsal root ganglia, DRGs) as a model, we show that neurogenesis also occurs in the peripheral nervous system, but in a manner different from that in the central nervous system. Satellite glial cells (SGCs) express the neuronal precursor markers Nestin, POU domain, class 4, transcription factor 1, and p75 pan-neurotrophin receptor. Following sciatic nerve injury, the suppression of endogenous proBDNF by proBDNF antibodies resulted in the transformation of proliferating SGCs into doublecortin-positive cells in the DRGs. Using purified SGCs migrating out from the DRGs, the inhibition of endogenous proBDNF promoted the conversion of SGCs into neuronal phenotypes in vitro. Our findings suggest that SGCs are neuronal precursors, and that proBDNF maintains the SGC phenotype. Furthermore, the suppression of proBDNF signaling is necessary for neuronal phenotype acquisition by SGCs. Thus, we propose that peripheral neurogenesis may occur via the direct conversion of SGCs into neurons, and that this process is negatively regulated by proBDNF. [Display omitted] • The SGC phenotype is maintained by endogenous proBDNF. • DRG-SGCs may be multipotent neuronal precursors. • DRG-SGCs differentiate into sensory neuron-like phenotypes by inhibition of proBDNF. [ABSTRACT FROM AUTHOR]